Lung Adenocarcinoma Harboring Triple Rare EGFR Exon 18 Mutations Rapidly Developed Resistance to Multiple Therapies

Anticancer Section / Original Paper

Liu Y. · Wu Y. · Wu F. · Hu C.

Author affiliations

Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, China

Log in to MyKarger to check if you already have access to this content.

Buy FullText & PDF Unlimited re-access via MyKarger Unrestricted printing, no saving restrictions for personal use
read more

CHF 38.00 *
EUR 35.00 *
USD 39.00 *

Select

KAB

Buy a Karger Article Bundle (KAB) and profit from a discount!

If you would like to redeem your KAB credit, please log in.

Save over 20% compared to the individual article price.

Learn more

Access via DeepDyve Unlimited fulltext viewing Of this article Organize, annotate And mark up articles Printing And downloading restrictions apply

Select

Subscribe Access to all articles of the subscribed year(s) guaranteed for 5 years Unlimited re-access via Subscriber Login or MyKarger Unrestricted printing, no saving restrictions for personal use read more

Subcription rates

Select

* The final prices may differ from the prices shown due to specifics of VAT rules.

Article / Publication Details

First-Page Preview

Abstract of Anticancer Section / Original Paper

Received: January 21, 2022
Accepted: June 14, 2022
Published online: June 28, 2022

Number of Print Pages: 5
Number of Figures: 2
Number of Tables: 0

ISSN: 0009-3157 (Print)
eISSN: 1421-9794 (Online)

For additional information: https://www.karger.com/CHE

Abstract

There is no standard therapy for nonsmall-cell lung cancer harboring rare coexistent EGFR mutations. Here, we report a female patient who was diagnosed as lung adenocarcinoma with three mutations of G724S, E709K, and V689I in exon 18. The patient responded to, but also showed rapid development of resistance to multiple therapies, including a second-generation EGFR-TKI of afatinib, a platinum-based doublet chemotherapy, and a multiple target TKI of anlotinib. As such, she ended up with a short overall survival time. Further research is required to understand the resistance mechanism(s) of these complex gene mutations.

© 2022 S. Karger AG, Basel

References Chiu CH, Yang CT, Shih JY, Huang MS, Su WC, Lai RS, et al. Epidermal growth factor receptor tyrosine kinase inhibitor treatment response in advanced lung adenocarcinomas with g719x/l861q/S768I mutations. J Thorac Oncol. 2015;10(5):793–9. Cho JH, Lim SH, An HJ, Kim KH, Park KU, Kang EJ, et al. Osimertinib for patients with non-small-cell lung cancer harboring uncommon EGFR mutations: a multicenter, open-label, phase II trial (KCSG-LU15-09). J Clin Oncol. 2020;38(5):488–95. Li J, Wang Z, Groen HJM, Zhao J, Wang P, Zhang C, et al. Uncommon EGFR G724S mutations arise in non-small-cell lung cancer patients with acquired resistance to first-generation EGFR-TKIs. Lung Cancer. 2018;118:173–5. Yang JCH, Sequist LV, Geater SL, Tsai CM, Mok TSK, Schuler M, et al. Clinical activity of afatinib in patients with advanced non-small-cell lung cancer harbouring uncommon EGFR mutations: a combined post-hoc analysis of LUX-Lung 2, LUX-Lung 3, and LUX-Lung 6. Lancet Oncol. 2015;16(7):830–8. Yang JCH, Schuler M, Popat S, Miura S, Heeke S, Park K, et al. Afatinib for the Treatment of NSCLC harboring uncommon EGFR mutations: a database of 693 cases. J Thorac Oncol. 2020;15(5):803–15. Frega S, Conte P, Fassan M, Polo V, Pasello G. A triple rare E709K and L833V/H835L EGFR mutation responsive to an irreversible pan-HER inhibitor: a case report of lung adenocarcinoma treated with afatinib. J Thorac Oncol. 2016;11(5):e63–4. Zeng L, Zhang Y, Yang N. EGFR exon 18 DelE709_T710insD as an acquired resistance mechanism to afatinib in an advanced EGFR exon 18 E709H lung adenocarcinoma. J Thorac Oncol. 2018;13(6):e93–5. Lei L, Wang WX, Zhu YC, Li JL, Fang Y, Wang H, et al. Potential mechanism of primary resistance to icotinib in patients with advanced non-small cell lung cancer harboring uncommon mutant epidermal growth factor receptor: a multi-center study. Cancer Sci. 2020;111(2):679–86. Article / Publication Details

First-Page Preview

Abstract of Anticancer Section / Original Paper

Received: January 21, 2022
Accepted: June 14, 2022
Published online: June 28, 2022

Number of Print Pages: 5
Number of Figures: 2
Number of Tables: 0

ISSN: 0009-3157 (Print)
eISSN: 1421-9794 (Online)

For additional information: https://www.karger.com/CHE

Copyright / Drug Dosage / Disclaimer Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

留言 (0)

沒有登入
gif